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The COVID-19 puzzle: deciphering pathophysiology and phenotypes of a new disease entity #MMPMID33965003
Osuchowski MF; Winkler MS; Skirecki T; Cajander S; Shankar-Hari M; Lachmann G; Monneret G; Venet F; Bauer M; Brunkhorst FM; Weis S; Garcia-Salido A; Kox M; Cavaillon JM; Uhle F; Weigand MA; Flohe SB; Wiersinga WJ; Almansa R; de la Fuente A; Martin-Loeches I; Meisel C; Spinetti T; Schefold JC; Cilloniz C; Torres A; Giamarellos-Bourboulis EJ; Ferrer R; Girardis M; Cossarizza A; Netea MG; van der Poll T; Bermejo-Martin JF; Rubio I
Lancet Respir Med 2021[Jun]; 9 (6): 622-642 PMID33965003show ga
The zoonotic SARS-CoV-2 virus that causes COVID-19 continues to spread worldwide, with devastating consequences. While the medical community has gained insight into the epidemiology of COVID-19, important questions remain about the clinical complexities and underlying mechanisms of disease phenotypes. Severe COVID-19 most commonly involves respiratory manifestations, although other systems are also affected, and acute disease is often followed by protracted complications. Such complex manifestations suggest that SARS-CoV-2 dysregulates the host response, triggering wide-ranging immuno-inflammatory, thrombotic, and parenchymal derangements. We review the intricacies of COVID-19 pathophysiology, its various phenotypes, and the anti-SARS-CoV-2 host response at the humoral and cellular levels. Some similarities exist between COVID-19 and respiratory failure of other origins, but evidence for many distinctive mechanistic features indicates that COVID-19 constitutes a new disease entity, with emerging data suggesting involvement of an endotheliopathy-centred pathophysiology. Further research, combining basic and clinical studies, is needed to advance understanding of pathophysiological mechanisms and to characterise immuno-inflammatory derangements across the range of phenotypes to enable optimum care for patients with COVID-19.
|*COVID-19/immunology/physiopathology[MESH]
|*Multiple Organ Failure/etiology/physiopathology[MESH]